INPP5D Antibody

1. Overall evidence did not indicate that inositol polyphosphate-5-phosphatase (INPP5D) rs35349669 single nucleotide polymorphism play a role in the genetic predisposition to late-onset Alzheimer's disease (LOAD) in Chinese population. PMID:27750211
2. JARID1B directly bound to PI3K/AKT signaling inhibitor SHIP1 gene promoter and decreased SHIP1 gene expression. PMID:27584795
3. Study shows that SHIP1 activity is decreased in adult Crohn's disease (CD) patients either through reduced intrinsic enxymatic activity or reduced protein expression, and propose that in addition to ATG16L1, SHIP1 may contribute to the risk conferred by the 2q37 CD risk locus. PMID:28767696
4. results indicate that FcgammaRIIB is not uniquely able to promote membrane recruitment of SHIP, but rather modulates its function via formation of distinct signaling complexes. Membrane recruitment of SHIP via Syk-dependent mechanisms may be an important factor modulating immunoreceptor signaling. PMID:27456487
5. SHIP has a role in extracellular matrix accumulation via suppressing PI3K/Akt/CTGF signaling in diabetic kidney dise PMID:27965087
6. Loss of SHIP promotes lung inflammation and mammary tumor metastasis. PMID:26683227
7. SHIP levels and activity are lower in intestinal tissues and peripheral blood samples from patients with Crohn's disease, resulting in induction of Il1-beta. PMID:26481854
8. Underexpression of SHIP1 is associated with drug resistance in acute myeloid leukemia. PMID:25971362
9. ectopically expressed SHIP1 accumulates in nucleolar cavities and colocalizes with the tumor suppressor protein p53. PMID:25723258
10. Results show that expression of SHIP1 protein is targeted by miR-155 in acute myeloid leukemia (AML) suggesting it as an onco-miR. The miR-155/SHIP1/PI3K/AKT signaling pathway could play an important role in the pathogenesis of AML. PMID:25175984
11. Overexpression of miR-155 in the gouty synovial fluid mononuclear cells leads to suppress SHIP-1 levels and enhance proinflammatory cytokines. PMID:24708712
12. SLAMF7-triggered inhibition is mediated by a mechanism involving Src kinases, CD45, and SHIP-1 that is defective in MM cells PMID:25312647
13. The discovery and replication studies presented here show SHIP-1 to be a risk marker for acute ischemic stroke in the Chinese population, which appears to be a novel finding. PMID:24352714
14. High ship1 expression is associated with chronic lymphocytic leukemia. PMID:24914134
15. Tks5 is needed for breast carcinoma cell invadopodium precursor stabilization, where the phox homology (PX) domain of Tks5 interacts with PI(3,4)P2. SHIP2 arrival at the invadopodium precursor coincides with the onset of PI(3,4)P2 accumulation. PMID:24206842
16. Based on these observations, authors conclude that miR-155 modulates the neuroinflammatory response during Japanese encephalitis virus infection via negative regulation of SHIP1 expression. PMID:24522920
17. SHIP1 silencing opposes TIGIT/PVR-mediated inhibitory signaling and restores cytotoxicity of YTS cells. PMID:23154388
18. Mutation in the PxxP domain of SHIP affects cell migration and invasion ability of K562 cells through increased MMP-9 expression, FAK phosphorylation and NF-kappaB activation. PMID:22575191
19. inositol phosphatase SHIP-1 inhibits NOD2-induced NF-kappaB activation by disturbing the interaction of XIAP with RIP2 PMID:22815893
20. SHIP1 mutant P1039S which does not reduce PI3K/AKT signaling anymore is located in a PXXP SH3 domain consensus binding motif. PMID:22820502
21. data suggest that miR-155 and miR-210/SHIP-1/Akt pathways could serve as clinical biomarkers for disease progression, and that miR-155 and miR-210 might serve as novel therapeutic targets in myelodysplastic syndromes. PMID:22249254
22. The CD2AP/SHIP1 complex and Cbl are recruited to blood dendritic cell (DC) antigen 2 (BDCA2) and Fc fragment of IgE high affinity I receptor (FcepsilonR1)gamma complex after BDCA2 cross-linking in human primary plasmacytoid DCs. PMID:22706086
23. The identification of SHIP1 as a nuclear inositol 5 phosphatase adds another member of the phosphoinositide and inositol modulating molecules to the emerging network of inositide signaling in the nucleus. PMID:21864674
24. indentification of LyGDI as a binding partner of SHIP, associating inducibly with the SHIP/Grb2/Shc complex PMID:21695085
25. Actin polymerization, F-actin accumulation, and Wiskott-Aldrich symptom protein phosphorylation are enhanced in SHIP-1-deficient B cells in a Bruton's tyrosine kinase (Btk)-dependent manner. PMID:21622861
26. Data suggest that SHIP-1 might regulate changes in the cytoskeleton. PMID:21402888
27. wtSHIP gene can down-regulate Akt phosphorylation and up-regulate cell cycle related proteins in K562 cells. PMID:19954644
28. This review summarizes how SHIP participates in normal immune physiology or the pathologies that result when SHIP is mutated. SHIP can have either inhibitory or activating roles in cell signaling. PMID:21155837
29. miR-155 led to down-regulation of SHIP, showing that it specifically targets the SHIP 3'untraslated regions. PMID:20041145
30. The novel platelet adapter Dok-3 and the structurally related Dok-1 are tyrosine phosphorylated in an Src kinase-independent manner downstream of alphaIIbbeta3 in human platelets, leading to an interaction with SHIP-1. PMID:19682241
31. In B cell lymphoma, elevated levels of miR-155, and consequent diminished SHIP1 expression are the result of autocrine stimulation by TNFalpha. PMID:19890474
32. implicated as regulator of histamine release in basophils PMID:11692111
33. SHIP localization to membrane receptors and subsequent activation along with the observed inability of SHIP -/- neutrophils to exhibit enhanced apoptosis with the stimulus combination. PMID:11724799
34. Association of SHIP with releasability in human basophils. PMID:12217402
35. data demonstrate that CD16 engagement on NK cells induces membrane targeting and activation of SHIP-1, which acts as negative regulator of antibody-dependent cellular cytotoxicity function PMID:12393695
36. SHIP-1 contributes to degradation of phosphatidylinositol trisphosphate (PI(3,4,5)P3) in T cells and thus influences signaling away from PI(3,4,5)P3-dependent effectors toward effectors that are exclusively driven by phosphatidylinositol 3,4-bisphosphate. PMID:12421919
37. SHIP expression appears to be differently altered in the early and late stages of differentiation of BCR-ABL-transformed cells PMID:12829595
38. SHIP-1 and Lyn have roles in the negative regulation of M-CSF-R-induced Akt activation PMID:12882960
39. SHIP positively, rather than negatively, regulates in vitro membrane recruitment of pleckstrin homology domain-containing signaling proteins Bam32 and TAPP2, which therefore specify a distinct wave of phosphatidylinositol 3-kinase signaling in B cells. PMID:14688341
40. SHIP1 and Lyn have roles as negative regulators of integrin alpha(IIb)beta(3) adhesive and signaling function PMID:15166241
41. SHIP1 and SHIP2 interact preferentially with Tec and inactivate it by de-phosphorylation of local PtdIns 3,4,5-P(3) and inhibition of Tec membrane localization PMID:15492005
42. SHIP1 negatively regulates monokine-induced NK cell IFN-gamma production in vitro and in vivo and provide the first molecular explanation for an important functional distinction observed between CD56bright and CD56dim human NK subsets. PMID:15604218
43. SHIP has a negative regulatory role in TLR2-induced neutrophil activation and in the development of related in vivo neutrophil-dependent inflammatory processes, such as acute lung injury in transgenic mice. PMID:15944314
44. Heterologous activation of SHIP by non-G-protein-coupled receptor-mediated routes can impinge on PI3K-dependent signaling pathways activated by independently ligated G-protein-coupled chemokine receptors. PMID:16038794
45. SHIP1 is necessary for FcgammaRIIB to negatively regulate B cell activation. PMID:16406061
46. Upregulated in oral mucosa during chronic periodontitis compared to its level during gingival health. PMID:16428799
47. Study showed H2O2-induced IKK activation in leukemic cells is mediated by SHIP-1; Jurkat cells expressing SHIP-1 are more resistant to H2O2-induced apoptosis than parental cells, suggesting SHIP-1 has an important role in leukemic cell responses to ROS PMID:16619039
48. Our results indicate that SHIP1 is involved, in a Src kinase-dependent manner, in the early signaling events observed upon the cross-linking of CD32a in human neutrophils. PMID:16682172
49. SHIP phosphorylation in stimulated human basophils undergoes modest nonspecific desensitization that persists despite dissociation of the desensitizing antigen, resulting in an immunologic memory of prior stimulation. PMID:16818760
50. SHIP1 not only acts as a negative player in T-cell lines proliferation, but also regulates critical pathways, such as NF-kappaB (nuclear factor kappaB) activation. PMID:17371259

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HGNC: 6079

UNIGENE: Hs.262886

KEGG: hsa:3635

STRING: 9606.ENSP00000352575

OMIM: 601582